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I read with interest the letter titled “Molluscum contagiosum virus infection in benign cutaneous epithelial cystic lesions” published recently in this journal1 and wish to report an additional case observed in our department.

A 13-year-old male teenager had been followed over the past 4 years for a plaque of morphea of the right thigh, treated with local applications of clobetasol propionate cream. Despite this treatment, new morphea lesions continued to appear on the inguinal area and the abdomen. At the latest consultation in our department, the patient presented an 8-mm firm asymptomatic nodule on the right thigh. No similar lesions were found elsewhere. The lesion was excised under local anesthesia. Microscopically, the epidermis looked normal. The upper and mid dermis contained a roundish epithelial cyst with no visible connection with the epidermis (Fig. 1). Its wall was made of an epidermal-type epithelium containing a granular cell layer, and its content was made of loose lamellar keratin. Higher magnification showed cytoplasmic, granular, eosinophilic inclusions within keratinocytes of the cyst wall and abundant ovoid molluscum bodies within the lamellar keratin content of the cyst (Figs. 2, 3).

Molluscum contagiosum (MC) is a common self-limiting skin infection due to the molluscum contagiosum virus (MCV), a poxvirus of which 2 types exist (MCV1 and MCV2). Macroscopically, MC present usually as multiple, translucent, often umbilicated papules with a shiny surface measuring up to 5 mm. MCV infects epidermal keratinocytes and leads to the formation of pear-shaped epithelial downgrowing lobules that contain the characteristic molluscum bodies. MCV may rarely infect keratinocytes of the hair follicle infundibulum, producing lesions with a misleading aspect that manifest as deeply-seated waxy papules2 or inflamed comedones and abscesses.3 In a study of 42 MC, it was found that 31% of them showed direct continuity with components of the hair follicle.4 Much more rarely, MCV infection is found in an epidermoid cyst (EC) in the absence of typical (epidermal) MC.5-13 Fewer than 15 such cases have been so far published. The clinical aspect is misleading, mimicking usually an EC, so that the correct diagnosis is made on histological examination, especially when the lesion is solitary, as was the case in our patient.

It has been proposed that MC infection of an EC may be due to (1) coinoculation of MCV at the time of the formation of the cyst or (2) invasion of a preexisting EC by MCV via the ostium that connects the epidermis with the underlying EC.12 Conversely, it has been claimed that MCV may spread from an infected EC to the epidermis and produce clinically typical MC lesions.12 Because ECs derive mostly from the hair follicles, it is possible that the presence of an MCV infection within the wall of an EC is due to the infection of a preexisting hair follicle that secondarily undergoes cystic transformation, possibly favored by scratching. Regarding the patient reported here, the prolonged application of potent local steroids probably favored the development of MC, as happens in children with atopic dermatitis under local steroid treatment. Such patients may be prone to develop clinically atypical MC infection.

ECs derive from the superficial part of the hair follicles (infundibulum), which is histologically similar to the epidermis. It is therefore not surprising, even though rarely observed, that an EC may be affected by the same pathological processes as those affecting the epidermis. Aside from infection with MCV, these include infection with human papillomavirus14; inflammatory dermatoses such as lichen planus15; and various benign (seborrheic keratosis)16 or malignant tumors, including Bowen disease17 and squamous cell,18 basal cell,19 and Merkel cell carcinomas20 and Paget disease.21 Therefore, microscopic examination of all the lesions diagnosed as an EC is warranted, especially in patients under local or systemic immunosuppressive treatment.